Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects.

Postmenopausal osteoporosis (PMOP) is a common bone disease characterized by decreased bone density and increased bone fragility due to decreased estrogen levels. Qiangguyin (QGY) is transformed from the famous traditional Chinese medicine BuShen Invigorating Blood Decoction. In this study, we used QGY to treat PMOP. We observed that QGY significantly reduced fat accumulation in the chondro-osseous junction. However, its specific mechanism of action remains unclear. To determine the specific molecular mechanism of QGY, we explored the pharmacological mechanism by which QGY reduces fat accumulation in the chondro-osseous junction through network pharmacological analysis. The active components and targets related to PMOP and QGY were screened from different databases, forming a composition-target-disease network. Next, a comprehensive analysis platform including protein-protein interaction (PPI) network, Gene Ontology (GO) enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were established. The results revealed that QGY inhibits adipogenic differentiation by activating the mitogen-activated protein kinase (MAPK) signaling pathway, thus reducing the accumulation of fat in the chondro-osseous junction. For further verification. In vitro and in vivo experiments were carried out. Our data showed that QGY significantly reversed the high expression of fatty acid binding protein 4 (FABP4) and peroxisome proliferator-activated receptor γ (PPARγ). Further, QGY prevents fat accumulation by inhibiting the expression of p38. In summary, the results of this study suggested that QGY-induced phenotypic changes are related to the activation of the p38 MAPK signaling pathway.

Clinical Outcomes of Revision Total Knee Arthroplasty after High Tibial Osteotomy and Unicompartmental Knee Arthroplasty: A Systematic Review and Meta-Analysis.

As more high tibial osteotomy (HTO) and unicompartmental knee arthroplasty (UKA) are performed, orthopaedic surgeons realize that more HTO and UKA failures will require revision to total knee arthroplasty (TKA) in the future. To systematically evaluate the clinical outcomes of TKA after HTO and TKA after UKA, the Embase, PubMed, Ovid, Web of Science, and Cochrane Library databases were searched for studies investigating revision TKA after HTO and UKA published up to June 2021. RevMan version 5.3 was used to perform the meta-analysis. The revision TKA after HTO and revision TKA after UKA groups were compared in terms of operative time, range of motion (ROM), knee score, postoperative complications, postoperative infection, revision, and revision implants used. Nine studies were ultimately included in the meta-analysis. Results revealed that the knee score for the revision TKA after HTO group was better than that of the revision TKA after UKA group (MD 4.50 [95% CI 0.80-8.20]; p = 0.02). The revision TKA after HTO group had a lower revision rate (OR 0.65 [95% CI 0.55-0.78]; p < 0.00001) and fewer revision implants used (OR 0.11 [95% CI 0.05-0.23]; p < 0.00001). There were no statistical differences in operation time (MD -2.00 [95% CI -11.22 to 7.21]; p = 0.67), ROM (MD -0.04 [95% CI -3.69-3.61]; p = 0.98), postoperative complications (OR 1.41 [95% CI 0.77-2.60]; p = 0.27), or postoperative infections (OR 0.89 [95% CI 0.61-1.29]; p = 0.53). To conclude, the revision rate of revision TKA after UKA was greater, and more revision implants were required. It is important for orthopaedic surgeons to preserve bone during primary UKA.

QiangGuYin Modulates the OPG/RANKL/RANK Pathway by Increasing Secretin Levels during Treatment of Primary Type I Osteoporosis.

QiangGuYin (QGY) is a common Traditional Chinese medicine prescription for the treatment of osteoporosis. Previous clinical studies have found that QGY effectively improves bone mineral density (BMD) in postmenopausal women, but its underlying mechanism remains unclear. The osteoprotegerin (OPG)/receptor activator of nuclear factor kappa B ligand (RANKL)/receptor activator of nuclear factor kappa B (RANK) pathway is a classic pathway involved in osteoporosis. Secretin levels are a serum marker of osteoporosis, but their effect on the OPG/RANKL/RANK pathway has not been reported. Hence, we investigated the relationship between the OPG/RANKL/RANK pathway and secretin and further revealed the mechanism underlying the effect of QGY in the treatment of osteoporosis. Mice were divided into secretin knockdown, secretin overexpression, and corresponding control groups. Micro-computed tomography was used to detect BMD in different groups, and the results show that QGY significantly improved BMD in mice of the secretin knockdown group. To further verify this, the serum levels of OPG, RANKL, RANK, and secretin were measured by enzyme-linked immunosorbent assays, and femur levels of OPG, RANKL, RANK, and secretin were evaluated by real-time quantitative PCR and western blotting. The results show that the expression of OPG was inhibited and that of RANKL and RANK was increased in mice from the secretin knockdown group, whereas the expression of OPG was upregulated and that of RANKL and RANK was downregulated after QGY intervention. Therefore, QGY inhibited bone resorption by promoting the expression of secretin and modulating the OPG/RANKL/RANK pathway. In addition to the effect of QGY, we also revealed the general regulatory effect of secretin on the OPG/RANKL/RANK pathway. We conclude that QGY modulates the OPG/RANKL/RANK pathway by increasing secretin levels during treatment of primary type I osteoporosis. This work provides a theoretical basis for the clinical use of QGY in the treatment of osteoporosis.